Israeli scientists have discovered that a single gene in skin cells not only builds the skin’s physical barrier but also coordinates its immune defenses, revealing the skin as an active, synchronized organ rather than a passive shield, Ben-Gurion University of the Negev announced. The findings offer new insights into inflammatory skin diseases such as psoriasis and atopic dermatitis, according to TPS-IL.
The epidermis, the skin’s outermost layer, protects the body from pathogens, UV radiation, and harmful chemicals. Its defenses rely on two components: a physical barrier of epithelial cells and an immune barrier formed by specialized cells, including Langerhans cells. While scientists have long known that these systems communicate during development, how they are synchronized has remained unclear.
Now, researchers have identified a key gene, ZNF750, that coordinates both processes. The study, led by Dr. Idan Cohen and Prof. Roy Gazit from the Shraga Segal Department of Microbiology, Immunology and Genetics, shows that ZNF750 is expressed in epithelial cells — cells that line the surface of the body — enabling them to produce IL34, a protein essential for the development of Langerhans immune cells.
Langerhans cells are a special type of immune cell found in the skin, specifically in the epidermis, the outermost layer. They are part of the body’s first line of defense against pathogens such as bacteria, viruses, and fungi.
“The study is important for understanding the complexity of synchronized developmental processes involving different cells in the same tissue, and specifically for the development of the skin, which is essential for the protection of the human body,” Gazit explained. “It also provides insight into disorders of the skin barrier and common diseases such as psoriasis. In fact, it closes a circle with research conducted 20 years ago, during which the ZNF750 gene was first identified in a family of psoriasis patients.”
Cohen added, “Our findings help explain why structural defects in the skin are often accompanied by immune system dysfunction. They also point to new therapeutic directions, such as restoring key support signals to rebalance skin immunity.”
The discovery of ZNF750’s dual role could lead to new treatments for common inflammatory skin conditions. By targeting the pathway that allows epithelial cells to produce IL34 and support immune cell development, researchers may be able to rebalance skin immunity in patients with psoriasis or atopic dermatitis. The findings also explain why structural defects in the skin often appear alongside immune dysfunction, giving clinicians a clearer understanding of disease progression.
Beyond dermatology, the study also demonstrates that a single gene in one cell type can coordinate the development of an entirely different system, showing how tissues integrate multiple functions in a synchronized way. This concept could inform regenerative medicine and therapies in other organs, where ensuring different cell types develop in concert is critical for restoring proper function.
The study was published in the peer-reviewed Cell Reports.
